Akodad Mariama, Lattuca Benoît, Nagot Nicolas, Georgescu Vera, Buisson Mathilde, Cristol Jean-Paul, Leclercq Florence, Macia Jean-Christophe, Gervasoni Richard, Cung Thien-Tri, Cade Stéphane, Cransac Frédéric, Labour Jessica, Dupuy Anne-Marie, Roubille François
UFR de médecine, cardiology department, hôpital Arnaud-de-Villeneuve, université Montpellier 1, CHU de Montpellier, 371, avenue du Doyen-Gaston-Giraud, 34295 Montpellier cedex 05, France.
UFR de médecine, medical information department, université Montpellier 1, CHU de Montpellier, 34295 Montpellier, France.
Arch Cardiovasc Dis. 2017 Jun-Jul;110(6-7):395-402. doi: 10.1016/j.acvd.2016.10.004. Epub 2017 Jan 3.
Inflammation is involved during acute myocardial infarction, and could be an interesting target to prevent ischaemia-reperfusion injuries. Colchicine, known for its pleiotropic anti-inflammatory effects, could decrease systemic inflammation in this context.
To evaluate the impact of colchicine on inflammation in patients admitted for ST-segment elevation myocardial infarction (STEMI).
All patients admitted for STEMI with one of the main coronary arteries occluded, and successfully treated with percutaneous coronary intervention, were included consecutively. Patients were randomized to receive either 1mg colchicine once daily for 1 month plus optimal medical treatment or optimal medical treatment only. C-reactive protein (CRP) was assessed at admission and daily until hospital discharge. The primary endpoint was CRP peak value during the index hospitalization.
Forty-four patients were included: 23 were treated with colchicine; 21 received conventional treatment only. At baseline, both groups were well balanced regarding age, sex, risk factors, thrombolysis in myocardial infarction flow and reperfusion delay. The culprit artery was more often the left anterior descending artery in the colchicine group (P=0.07), reflecting a more severe group. There was no significant difference in mean CRP peak value between the colchicine and control groups (29.03mg/L vs 21.86mg/L, respectively; P=0.36), even after adjustment for type of culprit artery (26.99 vs 24.99mg/L, respectively; P=0.79).
In our study, the effect of colchicine on inflammation in the context of STEMI could not be demonstrated. Further larger studies may clarify the impact of colchicine in acute myocardial infarction.
炎症在急性心肌梗死过程中起作用，可能是预防缺血再灌注损伤的一个有意义的靶点。秋水仙碱以其多效抗炎作用而闻名，在此背景下可减轻全身炎症。
评估秋水仙碱对ST段抬高型心肌梗死（STEMI）患者炎症的影响。
连续纳入所有因主要冠状动脉闭塞而入院并成功接受经皮冠状动脉介入治疗的STEMI患者。患者被随机分为两组，一组每天服用1mg秋水仙碱，持续1个月，同时接受最佳药物治疗；另一组仅接受最佳药物治疗。入院时及每天直至出院时评估C反应蛋白（CRP）。主要终点是本次住院期间CRP的峰值。
共纳入44例患者：23例接受秋水仙碱治疗；21例仅接受常规治疗。基线时，两组在年龄、性别、危险因素、心肌梗死溶栓血流和再灌注延迟方面均衡良好。秋水仙碱组罪犯血管更常为左前降支（P=0.07），提示该组病情更严重。秋水仙碱组与对照组的平均CRP峰值无显著差异（分别为29.03mg/L和21.86mg/L；P=0.36），即使在对罪犯血管类型进行调整后（分别为26.99mg/L和24.99mg/L；P=0.79）也是如此。
在我们的研究中，未证实秋水仙碱对STEMI患者炎症有影响。进一步的大型研究可能会阐明秋水仙碱在急性心肌梗死中的作用。
